Scientists discover why exercise reverses muscle aging
Key Points:
- Researchers from Duke-NUS, Singapore General Hospital, and Cardiff University found that exercise helps correct an imbalance in aging muscle cells caused by elevated DEAF1 gene levels, which disrupt protein maintenance and accelerate muscle deterioration.
- The study revealed that DEAF1 increases with age due to declining FOXO protein activity, driving excessive mTORC1 pathway activation that favors protein production over removal, leading to muscle weakening.
- Exercise lowers DEAF1 levels by activating proteins that restore balance in muscle repair mechanisms, allowing aging muscles to clear damaged proteins and rebuild strength, though very high DEAF1 or low FOXO levels may limit exercise benefits in some older adults.
- Findings confirmed in fruit flies and mice suggest DEAF1’s conserved role in muscle aging and highlight its potential as a therapeutic target to mimic exercise benefits, aiding muscle recovery in aging, surgery, illness, or chronic disease.
- This research advances understanding of muscle aging at the molecular level and could lead to new interventions to preserve muscle function and improve quality of life for aging populations globally.